Question 18

Regarding new-onset atrial fibrillation in a patient with sepsis in the ICU:
a) List six risk factors for new-onset atrial fibrillation in the critically ill patient who has NOT had cardiac surgery. (2 marks)
b) Discuss strategies for the reversion of rhythm and rate in new-onset atrial fibrillation in the critically ill. (8 marks)

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College answer

Syllabus topic/section:

2.1.3 Sepsis and Infections: L1
2.1.4 Cardiovascular Intensive Care / Cardiac arrhythmias: L1

Discussion:  

Candidates are reminded to read the question carefully: the question asked for a discussion of strategies for rate AND rhythm. Many candidates read the question as rate OR rhythm.
Candidates are reminded to become familiar with the glossary of terms. “Discuss” requires a detailed articulation of the subject. Good answers had details, discussed advantages and disadvantages of each strategy, and included precise answers of non-pharmacological strategies that were not just limited to DC cardioversion. For instance, a discussion of strategies to modulate sympathetic tone such as withdrawal of beta sympathomimetic agents, e.g., cease or reducing adrenaline/ dobutamine, weaning salbutamol as able, use of analgesia and sedation, normalising CO2, aiming for euvolaemia and minimising rapid fluid shifts displayed the standard required and was rewarded.

Discussion

"A detailed articulation of the subject" is not something one is usually capable of in writing, as to be perfectly correct "articulation" refers either to the production of intelligible speech, or the matching connection of coursework between institutions, or the mobile connection between body segments. That notwithstanding, the "discuss" vocabulary term does mean that some advantages, disadvantages and controversies need to be opened in the answer, and there are eight marks allocated, which suggests that the level of expected detail is substantial.

Well, at least a) is easy. Any of these would have been suitable:

Causes of Atrial Fibrillation Organised by System

Vascular:

  • Myocardial infarction
  • Pulmonary embolism
  • Pulmonary hypertension
  • Subarachnoid haemorrhage

Infectious:

  • Sepsis
  • Myocarditis
  • Pericarditis
  • Infective endocarditis

Neoplastic:

  • Cardiac mass, eg. myxoma

Drug-induced:

  • Catecholamines
  • Alcohol
  • Caffeine

Idiopathic:

  • Infiltrative disease, eg. amyloidosis
  • Age-related fibrotic changes

Idiopathic:

  • Infiltrative disease, eg. amyloidosis
  • Age-related fibrotic changes

Congenitial:

  • Atrial septal defect
  • Familial AF

Autoimmune:

  • Autoimmune myocarditis

Traumatic:

  • Cardiac contusion
  • Cardiac surgery

Endocrine/environmental:

  • Hypothermia
  • Hyperthyroidism
  • Haemochromatosis/iron overload
  • Phaeochromocytoma
  • Electrolyte derangement

Now, Strategies for the reversion of rhythm and rate in new-onset atrial fibrillation in the critically ill: how would you even structure this? The usual approach would not be suitable (advantages, disadvantages, controversies) because there are a lot of options to discuss. The unprepared trainee would flounder without a scaffold. What follows hopefully helps:

  • Decision re. endpoints
    • Rhythm control is preferred where:
      • The initiating factors are well controlled
      • The patient is already sedated and ventilated (for DCCV)
      • The AF is recent in onset (<24-48 hrs)
      • The bleeding risk is high (anticogulation is contraindicated)
      • The AF is haemodynamically significant
      • The patient has no structural heart disease, eg. atrial enlargement
    • Rate control is preferred where
      • The patient has structural cardiac disease that makes sustained cardioversion unlikely
      • The stimulus for the AF remains active
      • The AF is of unknown duration and TOE is impossible or difficult
    • Rate goals are a HR of ~ 110 for most patients, or ~80 for those with decreased LV function (AHA 2023)
  • Minimise arrhythmogenic stimuli
    • Correct electrolytes (magnesium and potassium)
    • Wean the inotropes/bronchodilators or reduce the diuretics
    • Remove mechanical stimuli (eg. PA catheter, pleural effusion)
    • Reducing the sympathetic tone:
      • Address pain and agitation
      • Reversing the shock, eg. replace volume
      • Correct hypercapnia or acidosis
      • Extubate (or, reintubate) the patient.
  • Rate control options
    • Haemodynamically ​​​​​​stable patients: β-blockers and calcium channel blockers
    • Unstable patients: ​Class III antiarrhythmic agents such as​​​​​​ amiodarone vernakalant and ibutilide are the next best option, and preferred in unstable patients
    • Digoxin can be added in either scenario, but:
      • less effective where the sympathetic tone is high
      • Relies on renal clearance
  • Rhythm control options
    • Electrical cadioversion is an option for haemodynamically unstable patients 
    • In practice, often return to sinus rhythm is not sustained unless the underlying cause is addressed
    • Pharmacological cardioversion with Class III antiarrhythmics in not mutually exclusive with rate control and can be pursued concurrently as a desirable outcome of amiodarone therapy